You get a cut and you start bleeding. But after a little while, the bleeding stops. That stopping of the flow of blood is called hemostasis.
When you get a cut, this causes damage to the walls of the blood vessels in that area. As a result, blood will escape through the damaged vessel and that’s what you experience as bleeding.
If you keep on bleeding for too long, that’s eventually going to result in anemia, which has a whole host of issues that come along with it as we discussed in my post on red blood cell disorders.
Three Basic Steps of Hemostasis
We have to prevent that from happening and we want the tissue to actually heal. This hemostasis involves three processes. The first is vascular spasm, the second is platelet plug formation and the third is coagulation. Let’s break these down individually.
First, let’s deal with vascular spasm. This is also called vasoconstriction.
If we look at the structure of the walls of our blood vessels, we see that the middle layer contains smooth muscle. Anytime you see muscle you know that contraction can take place.
In this case, in response to the damaged wall of the blood vessel, the smooth muscle layers will start contracting. This is called vascular spasm. Here’s why this happens.
When there’s a cut, there are pain receptors that release chemicals in that local area. Also, the cells that are lining the inner layer of the blood vessel wall also release chemicals. Those chemicals will cause the smooth muscle to contract and that action will then help to restrict the flow of blood.
It’s like if you have a hose and you squeeze the hose – that limits the flow of water. It’s the same thing here. So that’s the first step – vascular spasm. Let’s slow down the flow of blood.
Platelet Plug Formation
Then, there’s the formation of the platelet plug. In the last article, we spoke about platelets and how they play a significant role in hemostasis. That’s a great introduction to what we’re talking about here. But essentially, we have these platelets that are in the blood that freely travel through the blood vessels for moments like this.
Well, when there’s damage to the blood vessel, it exposes the underlying connective tissue and collagen fibers that’s normally in the walls of the blood vessels.
As these platelets are passing by minding their own business, they get activated and change their shape. They also will release granules and the result is that they become spiked and sticky. So they clump together around the damaged tissue to form what’s called a platelet plug.
This entire process is helped by a glycoprotein that’s found in the blood called von Willebrand factor. It helps to stabilize the platelet plug. This is like a temporary internal bandaid helping to stop the flow of blood until we can have something more permanent.
And what’s also cool is that as the plug forms, the platelets also release a few other substances that help the process even more. They release ADP – adenosine diphosphate. This helps to attract even more platelets to the site of injury.
They also release serotonin, which has various functions but in this situation, it stimulates and helps to maintain the vasoconstriction we spoke about earlier.
Some other substances that are released are prostaglandins and phospholipids – they help to maintain vasoconstriction as well, but also help to activate other clotting factors. We’ll talk about that in a sec.
For the third and final process, we have coagulation – also known as clotting. We are forming a blood clot. Yayyyyy!
Now, this is a process that involves a complex cascade of events that involves a bunch of clotting factors. The goal of this process is to form a fibrin mesh that holds the platelet plug in place so that healing can take place as efficiently as possible.
Here’s a simplified look at how this happens.
I mentioned that there’s a complex cascade of events. In that cascade, there are two pathways – an intrinsic pathway and an extrinsic pathway. They both involve various clotting factors.
Intrinsic and Extrinsic Pathways of Blood Coagulation
The intrinsic pathway gets activated as a result of the damage to the wall of the blood vessel – hence the name intrinsic – it’s a pathway that’s within the blood vessel.
The extrinsic pathway happens as a result of the damage to the extravascular cells – those not a part of the blood vessels. They’re outside the blood vessels – hence the name extrinsic.
Common Pathway of Blood Coagulation
Now both of those pathways lead to the common pathway. And here’s the important part.
Well, it’s all-important, but the key thing here – the main goal is that in the common pathway, there’s an inactive enzyme called prothrombin. That gets converted to the active enzyme thrombin.
Once this thrombin is active, it converts fibrinogen, which is soluble and inactive into fibrin, which is insoluble and active. Those fibrin strands will form that fibrin mesh that we spoke about earlier that holds everything in place so that healing can happen.
So ultimately, for hemostasis to happen, first we want to slow down the flow of blood, and the vascular spams accomplish this. Then, we get the platelet plug formation and lastly – coagulation, resulting in the fibrin mesh holding everything together.
That’s it for Hemostasis. But if you’re curious about blood types and the physiology behind all of that, check out this post.